Craig Hodges, PhD

Contact Information

10900 Euclid Ave, BRB 725

Cleveland, OH 44106

Phone: 216-368-0008

Fax: 216-368-4223



Craig Hodges, PhD

Assistant Professor

  • Division: Pulmonology, Allergy and Immunology


Dr. Hodges received his B.S. in Biology from Berry College in 1996 and his Ph.D. in Genetics from Case Western Reserve University in 2002. His graduate training was in the laboratory of Dr. Patricia Hunt where his studies focused on the genetics of chromosome segregation during meiosis and infertility using mouse models. Dr. Hodges then undertook postdoctoral training with Dr. Steven Stice at the University of Georgia studying early embryo dysfunction of clones from nuclear transfer using pigs and cows as model systems. Dr. Hodges returned to Case Western Reserve University to train with Dr. Terry Hassold using mouse models to study chromosome segregation and reproduction. In 2005, Dr. Hodges joined the laboratories of Dr. Mitchell Drumm and Dr. Mark Palmert in which he created two conditional Cftr mouse models that are currently being used to study various aspects of the disease Cystic Fibrosis. Dr. Hodges joined the faculty of the Department of Pediatrics at Case Western Reserve University in 2009.

Research Interests
Cystic Fibrosis (CF) is a systemic disease affecting many parts of the body including pulmonary, gastrointestinal, pancreatic, immune, endocrine and reproductive systems. With this in mind, we are interested in determining the extent to which specific cell types contribute to CF disease characteristics, whether the pathophysiology can be halted or reversed by CFTR functional correction and understanding the molecular mechanisms behind the physiological consequences of CFTR’s absence. We are beginning to address these issues through the use of traditional CF mouse models as well as recently created CF mouse models that allow for the conditional inactivation or restoration of Cftr function in specific tissues, cell types as well as at specific developmental time points. My laboratory is particularly interested in how the loss of CFTR leads to the intestinal dysfunction and reduced growth phenotypes associated with CF. We have found that these two phenotypes seem to be independent of each other in the CF mouse and we are investigating this further utilizing our CF models. In addition, we are examining how specific Cftr expressing cell types in the intestine contribute to CF intestinal dysfunction and understanding how modifier genes of intestinal dysfunction modulate disease which may lead to better treatments for CF.